Inflammation of the supporting tissues of the teeth characterized by apical migration of the junctional epithelium, loss of periodontal attachment, and loss of alveolar bone. The clinical features include purplish-red swollen (oedematous) and shiny gingival tissue, detachment of the interdental papillae, an increase in the gingival crevice (sulcus) beyond 3mm (periodontal pocket), usually no pain or discomfort, and bleeding on gentle probing. There may also be exudation of pus on digital pressure or probing, tooth mobility, drifting of the teeth, tooth loss, and gingival recession. Subgingival calculus is frequently present and causes additional irritation. The initiation of chronic periodontitis is thought to be due to gene polymorphism, which causes a change in the behaviour of cytokines, substances which influence the immune system. Histologically there is extensive destruction of collagen tissue and there may be fibrosis of the tissue outside the inflamed area. Many bacterial species have been identified, including Porphyromonas gingivalis, Bacillus forsythius, and Treponema denticola, although their role in the disease process is not clearly defined. General risk factors include smoking, which reduces the gingival blood circulation, diabetes, stress, leukaemia, and hormonal changes such as puberty, pregnancy, and the menopause. Local risk factors include the presence of calculus, malpositioned teeth, poorly constructed restorations, removable partial dentures, poor tooth contact areas, and a deep overbite causing direct gingival trauma. Treatment is by the removal of surface deposits, oral hygiene instruction, and addressing any predisposing risk factors. See also gingivitis.